Abstract

Introduction: Alteration in the glucose homeostasis is still the major cause of morbidity and mortality in the newborns. Intrauterine undernutrition plays an important role in causing adult insulin resistance and diabetes but the exact cause is still unknown.
Aim: To estimate the plasma glucose, serum insulin and cortisol levels at birth in newborns at different gestational age.
Materials and Methods: The present cross-sectional study conducted from December 2014 to June 2015 included 58 newborns enrolled as per the inclusion criteria and further categorized into Group I (very preterm; n=19; gestational age < 32 weeks), Group II (late preterm; n=20; gestational age between 32-37 weeks) and Group III (full term; n=19; gestational age >37 weeks) newborns. Venous Cord Blood (VCB) was collected and plasma glucose was analysed by GOD-POD (Glucose Oxidase-Peroxidase) method in auto analyser whereas serum insulin and cortisol were analysed by ELISA (Enzyme Linked Immunosorbent Assay). HOMA2-IR (Homeostatic Model Assessment) calculator was used to assess insulin resistance. All parametric data was expressed as mean±SD and analysed using ANOVA with Tukey’s as the Post-Hoc test. Correlation analysis was done using Pearson’s correlation co-efficient with scatter plot as the graphical representation.
Results: Significantly increased insulin and HOMA2-IR levels were found in group I (13.7±4.7μIU/mL and 1.6±0.58 respectively) when compared to group II (8.3±2.9μIU/mL and 0.93±0.2 respectively) and group III (8.3±2.1μIU/mL and 1.03±0.26 respectively). A positive correlation between cortisol levels and gestational age (r = 0.6, n = 58, p < 0.001) and a negative correlation between insulin and gestational age (r = -0.654, n = 58, p < 0.001) was observed in the study population.
Conclusion: Increased levels of insulin and HOMA2-IR as seen in the very preterm newborns signify the predisposition of these newborns to development of diabetes in later stages of life. The inverse association of cortisol and insulin with gestational age suggests that cortisol could also be responsible for impaired β cell function and insulin sensitivity.